Haverinen Jaakko, Vornanen Matti
Department of Biology, University of Joensuu, PO Box 111, 80101 Joensuu, Finland.
Am J Physiol Regul Integr Comp Physiol. 2007 Feb;292(2):R1023-32. doi: 10.1152/ajpregu.00432.2006. Epub 2006 Sep 28.
The hypothesis of pacemaker level origin of thermal compensation in heart rate was tested by recording action potentials (AP) in intact sinoatrial tissue and enzymatically isolated pacemaker cells of rainbow trout acclimated at 4 degrees C (cold) and 18 degrees C (warm). With electrophysiological recordings, the primary pacemaker was located at the base of the sinoatrial valve, where a morphologically distinct ring of tissue comprising myocytes and neural elements was found by histological examination. Intrinsic beating rate of this pacemaker was higher in cold-acclimated (46 +/- 6 APs/min) than warm-acclimated trout (38 +/- 3 APs/min; P < 0.05), and a similar difference was seen in beating rate of isolated pacemaker cells (44 +/- 6 vs. 38 +/- 6 APs/min; P < 0.05), supporting the hypothesis that thermal acclimation modifies the intrinsic pacemaker mechanism of fish heart. Inhibition of sarcoplasmic reticulum (SR) with 10 microM ryanodine and 1 microM thapsigargin did not affect heart rate in either warm- or cold-acclimated trout at 11 degrees C but reduced heart rate in warm-acclimated trout from 74 +/- 2 to 42 +/- 6 APs/min (P < 0.05) at 18 degrees C. At 11 degrees C, a half-maximal blockade of the delayed rectifier K+ current (I(Kr)) with 0.1 microM E-4031 reduced heart rate more in warm-acclimated (from 45 +/- 1 to 24 +/- 5 APs/min) than cold-acclimated trout (56 +/- 3 vs. 48 +/- 2 APs/min), whereas I(Kr) density was higher and AP duration less in cold-acclimated trout (P > 0.05). Collectively, these findings suggest that a cold-induced increase in AP discharge frequency is at least partly due to higher density of the I(Kr) in the cold-acclimated trout, whereas contribution of SR Ca2+ release to thermal compensation of heart rate is negligible.
通过记录完整的窦房组织和经酶分离的虹鳟鱼起搏细胞的动作电位（AP），对心率热补偿的起搏器水平起源假说进行了测试。这些虹鳟鱼分别适应4℃（冷）和18℃（暖）的环境。通过电生理记录，发现主要起搏点位于窦房瓣基部，组织学检查发现此处有一个形态上独特的由心肌细胞和神经成分组成的组织环。该起搏器的固有搏动频率在冷适应的虹鳟鱼（46±6次动作电位/分钟）中高于暖适应的虹鳟鱼（38±3次动作电位/分钟；P<0.05），在分离的起搏细胞搏动频率中也观察到类似差异（44±6次动作电位/分钟对38±6次动作电位/分钟；P<0.05），支持了热适应会改变鱼类心脏固有起搏机制的假说。用10微摩尔的兰尼碱和1微摩尔的毒胡萝卜素抑制肌浆网（SR），在11℃时对暖适应或冷适应的虹鳟鱼心率均无影响，但在18℃时，可使暖适应虹鳟鱼的心率从74±2次动作电位/分钟降至42±6次动作电位/分钟（P<0.05）。在11℃时，用0.1微摩尔的E-4031对延迟整流钾电流（I(Kr)）进行半数最大阻断，对暖适应虹鳟鱼心率的降低作用（从45±1次动作电位/分钟降至24±5次动作电位/分钟）比对冷适应虹鳟鱼更明显（56±3次动作电位/分钟对48±2次动作电位/分钟），而冷适应虹鳟鱼的I(Kr)密度更高，动作电位时程更短（P>0.05）。总的来说，这些发现表明，冷诱导的动作电位放电频率增加至少部分是由于冷适应虹鳟鱼中I(Kr)密度较高，而SR Ca2+释放对心率热补偿的贡献可忽略不计。
